A study published this month in the journal PLoS One shows that how quickly an HIV infection turns into AIDS is linked to a specific set of human genes as well as certain genes of the virus. The research confirms earlier studies that showed human genetics can be important for disease progression. The new research also shows more clearly how genes of the virus influence HIV infection.

HIV infections can vary widely in the amount of time they take to cause symptoms or turn into AIDS. For some people, called long-term non-progressors, the virus takes more than 10 years to show any symptoms, even without treatment.

For other people, called chronic progressors, HIV infections turn into AIDS within 10 years if not treated, and for rapid progressors, HIV infection progresses to AIDS within 3 years.

Previous studies had shown that some long-term non-progressors have protective gene variants that can slow down HIV infections.

In this study, researchers wanted to see if, in general, people’s genes – especially whether or not they have the protective gene variants – would affect the rate at which their HIV infection progressed.

For the study, scientists looked at 64 patients from all three categories – long-term non-progressors, chronic progressors, and rapid progressors – who had never received antiretroviral drugs. The researchers collected information on participants’ genetics and the HIV virus that had infected them.

They compared this information to how long their HIV infection had taken to progress to the point that antiretroviral therapy was needed.

The results showed a continuous loss of protective genes and an increase in risky genes from non-progressors to rapid progressors.

“Our study has demonstrated that the differences between [patient] groups are supported by virologic and [patient] genetic factors,” said Dr. Cecilio Lopez-Galindez, a lead investigator of the study, in email correspondence with The AIDS Beacon.

Genes that are known to offer protection from HIV infection include, for example, a certain set of variants of the HLA-B gene, which are well known to slow down HIV infections.

The researchers showed that these protective variants were found about 10 times more often in non-progressors than in rapid progressors.

The researchers noted that for two types of long-term non-progressors (viral controllers and viral non-controllers), patient genetics were not enough to completely explain their disease progression. Viral controllers have low viral loads, or amount of HIV in the blood, and viral non-controllers have higher viral loads but do not get sick.

To explain the difference between these two groups, they analyzed the characteristics of the viruses the participants were infected with. They found that viral controllers had HIV viruses that had not mutated as much as viruses in non-controllers.

Since mutations can only occur when the virus replicates, the researchers think that the lack of mutation is due to the fact that the virus is not multiplying as quickly. This could mean that some of the differences in rate of HIV disease progression depend on virus genes, and how well a particular HIV virus can replicate itself.

Dr. Amalio Telenti, a leader of the study and director of the Institute of Microbiology at the University of Lausanne, said the results could eventually help doctors determine who should start early treatment for HIV infection and who can wait.

“The pendulum is now swinging towards early treatment of most if not all patients,” said Dr. Telenti. “A possible use of [these results] would be to identify individuals who could defer treatment.”

Furthermore, knowing how and why the groups are different “could be very important for vaccine studies,” added Dr. Lopez-Galindez.

For more information, please see the article on the PLoS One website.